期刊
CURRENT BIOLOGY
卷 21, 期 11, 页码 990-997出版社
CELL PRESS
DOI: 10.1016/j.cub.2011.04.045
关键词
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资金
- National Institutes of Health [R01GM060396]
- National Science Foundation [MCB0918220]
- Chemical Sciences, Geosciences, and Biosciences Division of the Office of Basic Energy Sciences of the Department of Energy [DE-FG02-03ER15449]
- Deutsche Forschungsgemeinschaft (DFG) [SFB 670]
- SNF
- DFG
- Direct For Biological Sciences
- Div Of Molecular and Cellular Bioscience [0918220] Funding Source: National Science Foundation
- Grants-in-Aid for Scientific Research [23688044] Funding Source: KAKEN
Coordinated regulation of protection mechanisms against environmental abiotic stress and pathogen attack is essential for plant adaptation and survival. Initial abiotic stress can interfere with disease-resistance signaling [1-6]. Conversely, initial plant immune signaling may interrupt subsequent abscisic acid (ABA) signal transduction [7, 8]. However, the processes involved in this crosstalk between these signaling networks have not been determined. By screening a 9600-compound chemical library, we identified a small molecule [5-(3,4-dichlorophenyl)furan-2-yl]-piperidine-1-ylmethanethione (DFPM) that rapidly downregulates ABA-dependent gene expression and also inhibits ABA-induced stomatal closure. Transcriptome analyses show that DFPM also stimulates expression of plant defense-related genes. Major early regulators of pathogen-resistance responses, including EDS1, PAD4, RAR1, and SGT1b, are required for DFPM-and notably also for Pseudomonas-interference with ABA signal transduction, whereas salicylic acid, EDS16, and NPR1 are not necessary. Although DFPM does not interfere with early ABA perception by PYR/RCAR receptors or ABA activation of SnRK2 kinases, it disrupts cytosolic Ca2+ signaling and downstream anion channel activation in a PAD4-dependent manner. Our findings provide evidence that activation of EDS1/PAD4-dependent plant immune responses rapidly disrupts ABA signal transduction and that this occurs at the level of Ca2+ signaling, illuminating how the initial biotic stress pathway interferes with ABA signaling.
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